Processes coupling cardiac cell membrane excitation and contraction during cardiac hypertrophy induced by ventricular pressure overload are not completely understood. Previously, we demonstrated several changes in action potential configuration during the development of ventricular hypertrophy 3-120 days following the induction of chronic pressure overload of the right ventricle in cats. At 3 days, typically, there is a decrease in the action potential plateau voltage (away from zero potential) which returns to normal as hypertrophy progresses. We interpret the alteration in the action potential as representing a diminished cellular calcium influx during excitation and eventually this reduction in calcium influx may reduce cellular stores of calcium and cardiac contractility. Our current objectives include an in depth study of the relationship between the altered cardiac action potential plateau and mechanical activity, mapping the anatomical specificity of the electrical changes, and a temporal analysis of the electromechanical changes. We intend to evaluate the effects of drugs and ions on the depressed action potential plateau so as to determine possible mechanisms for its occurrence; agents currently used include increased extracellular calcium, catecholamine and selected ionophores. A final objective is to evaluate the effects of ionophores and digitalis on the myocardial electromechanical and hemodynamic parameters of those cats which ultimately exhibit cardiac failure. Techniques employed include microelectrode and isometric recording and high potassium-induced contracture in ventricular muscles from normal and sham-operated cats and cats killed at selected times following induction of pressure overload by chronic pulmonary artery occlusion.